"This research aimed to explore and better understand intervention protocols and their effect on lower limb control associated with anterior cruciate ligament (ACL) injury. A fundamental and unique aspect of this investigation was to establish a lab-based testing protocol that successfully mimicked actual game play. [...]This research validated a lab-based measure that best mimicked game-play to use as a pre- and post- testing measure for two common methods used in current ACL intervention strategies. In addition, further understanding of the effects of a landing training and dynamic balance training program were found." / Doctor of Philosphy

Bibliography: leaves 102-116. / 116, [43] leaves, [51] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Analyses the characteristics and relative incidence of annular defects in the human lumbar spine and investigates their role in the pathogenesis of invertebral disc degeneration. / Thesis (Ph.D.)--University of Adelaide, Dept. of Pathology, 1992

Two leaves of errata and addenda pasted into back pages. / Bibliography: leaves 174-208. / xix, 208 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis aimed to determine general roles for insulin-like growth factor binding proteins (IGFBPs) in regulating insulin-like growth factor-I (IGF-I) actions in wound repair. Preliminary experiments sought to characterise alterations to IGF-I levels and IGFBP profiles that may occur during wound repair. The effects that interactions with IGFBPs may have on IGF actions in wounds were addressed. Final experiments aimed to determine whether IGFBP-3 proteolysis observed in the initial work of the thesis acted to increase IGF bioavailablity. The results are discussed. / Thesis (Ph.D.)--University of Adelaide, Dept. of Surgery, 2000

Doctor of Philosophy / The general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.

[Truncated abstract] Shoulder injuries rank among the most prevalent and debilitating sustained by professional tennis players. The loads, or magnitude, location, direction, duration, frequency, variability and rate of force application, endured by tissues of the shoulder during stroke production, and more particularly the serve, are commonly implicated in shoulder joint injury (Chandler et al., 1992; McCann and Bigliani, 1994; Kibler, 1995). Indeed, past evidence points to these loads increasing along with serve velocity, as well as with varied segment use (Elliott et al., 2003). This dissertation therefore aimed to quantify hypothesised relationships between certain serve types and techniques, and shoulder joint loading among high performance able-bodied and wheelchair players. . . Of final note is that prospective 3D biomechanical examinations of shoulder joint motion in the tennis serve should consider placement of humeral triads distal to the biceps and/or triceps muscle belly. In comparison to markers placed at the mid-point of the humerus (i.e. as used in this thesis), these more distal triad positions appear to alleviate the spurious effects of soft tissue artefact thereby enhancing the accuracy of estimated long-axis rotation of the upper arm. Although the current representation of 3D humeral motion did not confound the comparisons made between serve types or techniques, it is likely that upper arm triads located just above the epicondyles of the humerus could have offered more insightful absolute comparisons to the literature. Further, the elaboration of a joint coordinate system at the shoulder to provide for the more meaningful and functional expression and interpretation of shoulder joint kinetic and kinematic data should also be central to all future, related investigative efforts.

[Truncated abstract] Osteoarthritis (OA) is the most common form of arthritis, characterized by progressively degeneration of articular cartilage. Chondrocyte is the only cell type in articular cartilage tissue and responsible for cartilage matrix turnover. This thesis focuses on the biological and genetic behaviors of human chondrocyte and potential therapeutic strategies that target on chondrocyte. Chondrocytes have been used for the tissue-engineered cartilage construction, especially in articular cartilage repair. The technique of chondrocyte-base tissue engineering utilizes in vitro propagated chondrocytes combined with several manufactured biomaterials to regenerate cartilage tissue. Although these technologies have been successfully applied in clinic, the biological characteristics of chondrocyte during in vitro propagation and after implantation remain unclear. This thesis reviewed the present studies of chondrocyte biology and its potential uses in tissue engineering. Particularly, chondrocytes have been shown to de-differentiate into fibroblastic-cells when they are exposed to inflammatory conditions or cultured on monolayer in vitro. This thesis investigated the gene expression profile of chondrocytes when they are cultured and serially passaged on monolayer in vitro. Human chondrocytes obtained from OA patients were cultured up to passage 6. Twenty-eight chondrocyte associated genes were measured by Real-time PCR. The results showed that a number of genes were changed in expression levels at various stages of passage as indications of chondrocyte de-differentiation. Chondrocytes derived from OA patients or normal donors exhibited a very similar gene expression pattern. Interestingly, transcription factor Sox-9, which plays a key role in chondrogenesis remained unchanged with increasing passage number, indicating that the de-differentiation process of chondrocyte is reversible. This thesis also focused on the development of novel pharmacological approaches for OA that target on articular chondrocyte. The clinical feature, etiology, pathogenesis, diagnostic approaches, conventional and potential future treatments for OA were briefly reviewed in this thesis. ... The effects of natural compounds on chondrocyte gene expression, proteoglycan degradation and nitric oxide production were measured. The results showed that parthenolide, a NF-kB inhibitor, regulated chondrocyte function by suppressing the up-regulation of gene expression of inflammatory factors and matrix proteinases induced by lipopolysaccharide, and down-regulating COX-2 expression. Parthenolide was able to reduce proteoglycan degradation in human chondrocytes, but had no effect on nitric oxide production. These results suggest that parthenolide mediates inflammatory-activated NF-kB pathway, and subsequently reduces inflammatory response, prevents cartilage destruction and relieves pain, and hence may be useful for OA treatment.

Tez (Tıpta Uzmanlık) - Süleyman Demirel Üniversitesi, Tıp Fakültesi, Acil Tıp Anabilim Dalı, 2004. / Bibliyografya var.

Diss. (sammanfattning) Linköping : Univ., 2004. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Thesis (M.D.)--Dept. of Surgery, University of Adelaide, 2001? / Includes bibliography (leaves 191-219).